Results 141 to 150 of about 185,542 (303)

The Evolutionary Trajectory and Prognostic Value of GITR+ Tregs Reprogramed by Tumor‐Intrinsic PD‐1/c‐MET Signaling in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
In pancreatic ductal adenocarcinoma (PDAC), tumor‐intrinsic PD‐1 signaling activates the MET pathway, leading to the establishment of an immunosuppressive tumor microenvironment (TME). This MET‐driven signaling cascade promotes the selective accumulation of GITR+ regulatory T cells (Tregs), a highly immunosuppressive subset.
Jiande Han   +16 more
wiley   +1 more source

Identification of Potential Common Molecular Factors of Pancreatic Cancer and Diabetes Mellitus using Microarray Data Analysis Combined with Bioinformatics Techniques and Experimental Validation

open access: diamond, 2021
Sima Kalantari   +9 more
openalex   +1 more source

The GGH/HuR Complex Binds and Stabilizes mRNAs to Maintain Tumor Cell Cycle and DNA Replication

open access: yesAdvanced Science, EarlyView.
Despite its canonical role in inhibiting DNA synthesis, GGH promotes tumor growth as a novel RNA‐binding protein. GGH binds GC‐rich 5′UTRs (e.g., CDC6/CCND1), recruits HuR to form a ternary complex that stabilizes mRNA via circular conformation, fueling DNA replication and the cell cycle. Targeting this axis suppresses NSCLC progression.
Yu Li   +9 more
wiley   +1 more source

Advanced Microfluidics for Single Cell‐Based Cancer Research

open access: yesAdvanced Science, EarlyView.
Cutting‐edge microfluidic platforms are transforming single‐cell cancer research. This review highlights advanced technologies, from droplet microfluidics to tumour‐chips, that enable functional and spatial single‐cell analyses. By integrating biosensing, immune components, and patient‐derived materials, these systems offer new insights into tumour ...
Adriana Carneiro   +10 more
wiley   +1 more source

Osteoblast‐CD4+ CTL Crosstalk Mediated by SIRT1/DAAM2 Axis Prevents Age‐Related Bone Loss

open access: yesAdvanced Science, EarlyView.
In the osteoblastic niche, SIRT1 activates and recruits CD4+ CTLs by increasing DAAM2 expression via EZH2 deacetylation and boosting the secretion of key chemokines, such as CCL3, CCL5, and CXCL10. Then, CD4+ CTL directly eliminates senescent osteoblasts in an MHC‐II‐dependent way, thereby slowing down the process of bone ageing and effectively ...
Bin Yang   +20 more
wiley   +1 more source

MALMPS: A Machine Learning‐Based Metabolic Gene Prognostic Signature for Stratifying Clinical Outcomes and Molecular Heterogeneity in Stage II/III Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
Chen et al. identified a metabolic gene prognostic signature with machine‐learning framework and assessed the prognostic value in independent CRC cohorts. The metabolic signature subtypes are characterized by specific metabolic and proteomic characteristics, and associated with distinct molecular pathway and therapeutic potential.
Hao Chen   +12 more
wiley   +1 more source

Targeting IGF1R Overcomes Armored and Cold Tumor Microenvironment and Boosts Immune Checkpoint Blockade in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
IGF1R is highly expressed in the armored & cold tumors, and collagen mediates IGF1R at the transcriptional and post‐translational levels to promote TNBC cell invasion and immune escape and to stabilize its own structure by interacting with the collagen receptor DDR1.
Mengyun Wan   +8 more
wiley   +1 more source

STAT6 Activation Exacerbates Ferroptosis in Airway Epithelium by Inhibiting PRKN‐Mediated Mitophagy in Pulmonary Fibrosis

open access: yesAdvanced Science, EarlyView.
This study uncovers STAT6‐driven pulmonary fibrosis (PF) via suppression of PRKN‐mediated airway epithelial mitophagy, triggering mitochondrial dysfunction and ferroptosis. Rifabutin is identified as a potent STAT6 inhibitor that effectively reverses fibrotic progression. These findings reveal the STAT6‐PRKN axis as a pathogenic regulator and provide a
Youjing Yang   +7 more
wiley   +1 more source

Home - About - Disclaimer - Privacy